No abstract available.
Organization and Administration* ; Psychotherapy*

Relatively little is known about the neurobiology of insomnia, despite its wide prevalence and broad medical impact. Although much is still to be learned about the pathophysiology of the disorder, identification, systematic assessment, and appropriate treatment are clearly beneficial to patients. Recent research, using quantitative EEG, polysomnography (PSG), multiple sleep latency test (MSLT) and neuroimaging techniques, suggests that some broad areas can be identified as possible pathophysiological models. Sleep-wake homeostat model hypothesizes a failure in homeostatic regulation of sleep, an attenuated increase in sleep drive with time awake, and/or defective sensing of sleep need. Circadian clock model hypothesizes a dysfunctional circadian clock, resulting in changes in the timing of sleep-wake propensity that are incompatible with normal sleep. Intrinsic sleep-wake state mechanism model suggests that abnormal function of insomnia comprises the systems responsible for expression of the sleep states themselves. Extrinsic over-ride mechanism (stress-response) model suggests that insomnia reflects the consequences of overactivity of one of the systems considered "extrinsic" to normal sleep-wake control. Many current therapies for insomnia are based on these physiological models. Several attempts have been made to create a physiological model that would explain this disorder and could be used as a foundation for treatment. However, it appeared that no model can fully explain and clarify all aspects of insomnia. Future research should be necessary to expand our knowledge on the biological dimensions of insomnia.
Circadian Clocks ; Electroencephalography ; Humans ; Neurobiology ; Neuroimaging ; Polysomnography ; Prevalence ; Sleep Initiation and Maintenance Disorders

No abstract available.
Movement Disorders* ; Prevalence*

No abstract available.
Organization and Administration* ; Psychotherapy*

The most common pathogen of respiratory tract infection among school-age children and adolescents is Mycoplasma pneumoniae, which causes clinical manifestations of pneumonia, acute asthmatic attack, pharygitis, and tonsilitis. It can also cause extrapulmonary infections that involves skin, the nervous system, the digestive system, the cardiovascular system, and the hematopoietic system. It is reported that the central nervous system symptoms may occur in 0.1% to 7% of patients hospitalized with Mycoplasma pneumoniae infection. Direct invasion, toxin, immune-mediated, and vascular phenomenon have been proposed for the etiology of the neurological manifestations. We have experienced a six-year-old male patient with Mycoplasma pneumoniae pneumonia who had complained of both leg pains and immobility two weeks after the onset of pneumonia, which was confirmed as peripheral neuropathy of Guillain-Barr syndrome. Three weeks after the disease-onset, altered consciousness and seizure attacks developed and intravenous immunoglobulins infused under the impression of encephalitis induced by Mycoplasma pneumoniae infection. He showed complete recovery of running and mentality five months after the disease-onset. We herein report a case of Mycoplasma pneumoniae pneumonia complicated with Guillain-Barr Syndrome and encephalitis about 2 or 3 weeks after the disease onset with a review of literatures.
Adolescent ; Cardiovascular System ; Central Nervous System ; Child ; Consciousness ; Digestive System ; Encephalitis* ; Guillain-Barre Syndrome* ; Hematopoietic System ; Humans ; Immunoglobulins ; Immunoglobulins, Intravenous ; Leg ; Male ; Mycoplasma pneumoniae* ; Mycoplasma* ; Nervous System ; Neurologic Manifestations ; Palatine Tonsil ; Peripheral Nervous System Diseases ; Pneumonia* ; Pneumonia, Mycoplasma* ; Respiratory Tract Infections ; Running ; Seizures ; Skin

OBJECTIVE: Panic disorder has been suggested to be divided into the respiratory and non-respiratory subtypes in terms of its clinical presentations. The present study aimed to investigate whether there are any differences in treatment response and clinical characteristics between the respiratory and non-respiratory subtypes of panic disorder patients. METHODS: Among the 48 patients those who completed the study, 25 panic disorder patients were classified as the respiratory subtype, whereas 23 panic disorder patients were classified as the non-respiratory subtype. All patients were treated with escitalopram or paroxetine for 12 weeks. We measured clinical and psychological characteristics before and after pharmacotherapy using the Panic Disorder Severity Scale (PDSS), Albany Panic and Phobic Questionnaire (APPQ), Anxiety Sensitivity Index-Revised (ASI-R), State-Trait Anxiety Inventory (STAI-T, STAI-S), Hamilton Anxiety Rating Scale (HAM-A), and Hamilton Depression Rating Scale (HAM-D). RESULTS: The prevalence of the agoraphobia was significantly higher in the respiratory group than the non-respiratory group although there were no differences in gender and medication between the two groups. The respiratory group showed higher scores on the fear of respiratory symptoms of the ASI-R. In addition, after pharmacotherapy, the respiratory group showed more improvement in panic symptoms than the non-respiratory group. CONCLUSION: Panic disorder patients with the respiratory subtype showed more severe clinical presentations, but a greater treatment response to SSRIs than those with non-respiratory subtype. Thus, classification of panic disorder patients as respiratory and non-respiratory subtypes may be useful to predict clinical course and treatment response to SSRIs.
Agoraphobia ; Anxiety ; Citalopram ; Classification ; Depression ; Drug Therapy ; Humans ; Panic ; Panic Disorder* ; Paroxetine ; Prevalence ; Surveys and Questionnaires ; Serotonin Uptake Inhibitors ; Treatment Outcome

OBJECTIVES : The present study aimed to compare anxiety sensitivity among anxiety disorder groups, and to examine the relationships between lower-order factors of anxiety sensitivity and each anxiety disorder. METHODS : Three hundred and twenty four normal control subjects and 212 patients with anxiety disorders were enrolled in this study. All subjects completed a psychometric assessment package including the Korean Anxiety Sensitivity Index-Revised (ASI-R) test. Statistical analysis of the two groups was performed using the Mann-Whitney U test, and comparison of anxiety sensitivity amongthe anxiety-disorder groups (panic disorder-PD, general anxiety disorder-GAD, social phobia- SP, obsessive-compulsive disorder-OCD) was investigated using Kruskal-Wallis test. RESULTS : All anxiety disorder groups showed higher total scores of the ASI-R than did the normal control group (Z=-13.724, p<.001), and the mean total score of the ASI-R in the panic disorder group was the highest among the anxiety disorder groups. The mean score of each lower-order factor of the ASI-R in each anxiety disorder group was higher than that of the normal control group and there were statistically significant differences in fear of cardiovascular symptoms (PD,GAD>SP,OCD), fear of respiratory symptoms (PD>GAD, SP,OCD), and fear of publicly observable anxiety reactions (SP>PD,OCD) among the anxiety disorder groups. CONCLUSION : These results suggest that anxiety sensitivity reflects vulnerability to anxiety disorders, and that lower-order factors of the ASI-R may help in the differential diagnosis of anxiety disorders.
Anxiety ; Anxiety Disorders ; Diagnosis, Differential ; Humans ; Panic Disorder ; Psychometrics

OBJECTIVES : The present study aimed to compare anxiety sensitivity among anxiety disorder groups, and to examine the relationships between lower-order factors of anxiety sensitivity and each anxiety disorder. METHODS : Three hundred and twenty four normal control subjects and 212 patients with anxiety disorders were enrolled in this study. All subjects completed a psychometric assessment package including the Korean Anxiety Sensitivity Index-Revised (ASI-R) test. Statistical analysis of the two groups was performed using the Mann-Whitney U test, and comparison of anxiety sensitivity amongthe anxiety-disorder groups (panic disorder-PD, general anxiety disorder-GAD, social phobia- SP, obsessive-compulsive disorder-OCD) was investigated using Kruskal-Wallis test. RESULTS : All anxiety disorder groups showed higher total scores of the ASI-R than did the normal control group (Z=-13.724, p<.001), and the mean total score of the ASI-R in the panic disorder group was the highest among the anxiety disorder groups. The mean score of each lower-order factor of the ASI-R in each anxiety disorder group was higher than that of the normal control group and there were statistically significant differences in fear of cardiovascular symptoms (PD,GAD>SP,OCD), fear of respiratory symptoms (PD>GAD, SP,OCD), and fear of publicly observable anxiety reactions (SP>PD,OCD) among the anxiety disorder groups. CONCLUSION : These results suggest that anxiety sensitivity reflects vulnerability to anxiety disorders, and that lower-order factors of the ASI-R may help in the differential diagnosis of anxiety disorders.
Anxiety ; Anxiety Disorders ; Diagnosis, Differential ; Humans ; Panic Disorder ; Psychometrics

Panic disorder is a common mental disorder that causes considerable disability. However, the etiology of panic disorder remains unclear. Preclinical neuroanatomical and neurophysiological studies have provided clues to the neurobiological basis of panic disorder, and recent developments in neurobiological techniques in neurochemical research, brain imaging, and genetic research provide a further understanding of anxiety, fear, and panic disorder. In this article, we introduce a functional neuroanatomic model of fear and anxiety, and consider the implications of recent developments and debates in neurobiological findings with respect to panic disorder.
Anxiety ; Genetic Research ; Mental Disorders ; Neurobiology ; Neuroimaging ; Panic ; Panic Disorder

Panic disorder is a common mental disorder that causes considerable disability. However, the etiology of panic disorder remains unclear. Preclinical neuroanatomical and neurophysiological studies have provided clues to the neurobiological basis of panic disorder, and recent developments in neurobiological techniques in neurochemical research, brain imaging, and genetic research provide a further understanding of anxiety, fear, and panic disorder. In this article, we introduce a functional neuroanatomic model of fear and anxiety, and consider the implications of recent developments and debates in neurobiological findings with respect to panic disorder.
Anxiety ; Genetic Research ; Mental Disorders ; Neurobiology ; Neuroimaging ; Panic ; Panic Disorder